期刊
BIOCHEMICAL GENETICS
卷 58, 期 5, 页码 783-800出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10528-020-09976-9
关键词
MIAT; miR-330-5p; TRAF6; NF-kappa B; LPS-induced sepsis; Cardiomyopathy
资金
- Project of Beijing Medical Health Public Welfare Foundation [B185040]
Sepsis is a whole-body inflammation and main cause of death in intensive care units worldwide. We aimed to investigate the roles of lncRNA MIAT and miR-330-5p in modulating inflammatory responses and oxidative stress in lipopolysachariden (LPS)-induced septic cardiomyopathy. Serum and heart tissue were collected from in vivo septic mice model, ELISA and qRT-PCR were used to measure the expression of pro-inflammation cytokines, MIAT and miR-330-5p, respectively. The knockdown of MIAT and overexpression of miR-330-5p were conducted to assess their effects on regulating inflammation response and intracellular oxidative stress in LPS-stimulated HL-1 cells. The reactive oxygen (ROS) level, mitochondrial membrane potential (MMP), GSH/GSSH ratio, and lipid peroxidation assessment (MDA) were used to evaluate the intracellular oxidative stress. Dual-luciferase reporter assay was performed to identify the association between MIAT and miR-330-5p, TRAF6 and miR-330-5p, respectively. In septic mice, the expression of MIAT and pro-inflammation cytokines was elevated while the expression of miR-330-5p decreased. Knockdown of MIAT or overexpression of miR-330-5p restrained inflammation and oxidative stress induced by LPS in vitro; MIAT directly targeted miR-330-5p to regulate NF-kappa B signaling, and miR-330-5p targeted against TRAF6 to suppress the activation of NF-kappa B signaling. We determined that lncRNA MIAT directly binds to miR-330-5p to activate TRAF6/NF-kappa B signaling axis and further promotes inflammation response as well as oxidative stress in LPS-induced septic cardiomyopathy. This finding suggests the potential therapeutic role of lncRNA MIAT and miR-330-5p in LPS-induced myocardial injury.
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